U.S. patent number 4,759,368 [Application Number 06/936,828] was granted by the patent office on 1988-07-26 for transcutaneous nerve stimulator.
This patent grant is currently assigned to Medical Designs, Inc.. Invention is credited to Richard J. Fisher, Jr., John P. Landino, John B. Spanton, Gregory A. Todd, Terry A. Todd.
United States Patent |
4,759,368 |
Spanton , et al. |
July 26, 1988 |
**Please see images for:
( Certificate of Correction ) ** |
Transcutaneous nerve stimulator
Abstract
A transcutaneous nerve stimulating device is provided having a
plurality of operating modes, namely burst, normal (single
amplitude/single pulse width), rate modulation, amplitude
modulation and strength-duration/rate modulation. In the lattermost
mode, the rate modulation control circuitry acts independently of
the inter-related amplitude and pulse width modulations to result
in a means of nerve stimulation obviating the phenomenon of
accommodation.
Inventors: |
Spanton; John B. (Sunbury,
OH), Todd; Gregory A. (Westerville, OH), Landino; John
P. (Westerville, OH), Todd; Terry A. (Canton, OH),
Fisher, Jr.; Richard J. (Sunbury, OH) |
Assignee: |
Medical Designs, Inc.
(Westerville, OH)
|
Family
ID: |
25469132 |
Appl.
No.: |
06/936,828 |
Filed: |
December 2, 1986 |
Current U.S.
Class: |
607/46; 607/63;
607/72; D24/200 |
Current CPC
Class: |
A61N
1/36021 (20130101) |
Current International
Class: |
A61N
1/36 (20060101); A61N 001/36 () |
Field of
Search: |
;128/421,422,423R |
References Cited
[Referenced By]
U.S. Patent Documents
Primary Examiner: Cohen; Lee S.
Attorney, Agent or Firm: Phillips; Patrick P.
Claims
Having thus described this invention, what is claimed is:
1. A transcutaneous nerve stimulating device which eliminates the
phenomenon of accommodation, comprising
a pulse generator means for generating a plurality of pulses,
interconnected amplitude, pulse width, and rate modulation control
means, which cause the amplitude, pulse width and rate of the
generated pulse to vary in a prescribed manner, said amplitude
control means interacting with said pulse width control means such
that a change in the pulse amplitude will effect an inverse change
in the pulse width, with pulse width decreasing when pulse
amplitude increases and with pulse width increasing when pulse
amplitude decreases, said rate modulation control means acting
independently of the relationship between said amplitude control
means and pulse width control means to modulate the rate of the
pulse generated, and
means for carrying said pulses to tissue engaging electrodes.
2. A device according to claim 1 wherein said generated pulse is
associated with a current flow which is allowed to bias Germanium
diodes as part of the circuitry of said device.
3. A device according to claim 1 wherein said amplitude, pulse
width and rate control means are electrically connected.
4. A device according to claim 1 wherein said prescribed manner
first includes the decreasing of the rate followed by its increase
back to the initial rate, and secondly the mutual interaction
between the amplitude control means and the pulse width control
means such that the pulse width is responsive to changes in
amplitude.
5. A device according to claim 4 wherein said rate decreases by
50%.
6. A device according to claim 4 wherein said mutual interaction
between said amplitude control means and said pulse width control
means causes the pulse width to increase by 40% responsive to a
decrease in the amplitude of 25%, followed by their return to their
initial values.
7. A device according to claim 6 wherein said mutual interaction
results in specific amplitude and pulse width values which if
plotted would the approximate A-gamma-motor curve strength-duration
associated with the nerve being stimulated.
8. A device according to claim 7 wherein said pulse width increases
in response to a decrease in amplitude until said pulse width
reaches the A-delta-pain line.
9. A device according to claim 4 wherein said prescribed manner has
a modulation cycle of six seconds, said modulation cycle being the
time of the rate modulation as well as the mutual interaction
between the pulse width control means and the amplitude control
means.
10. A device according to claim 1 which includes means for
additional modes of operation having pulses generated in other than
said prescribed manner, said additional modes including rate
modulation, amplitude modulation, single amplitude/single pulse
width and burst.
11. A device according to claim 1 wherein the prescribed manner
includes decreasing of the rate by 50%.
12. A device according to claim 11 wherein said prescribed manner
includes mutual interaction between said amplitude control means
and said pulse width control means which causes the pulse width to
increase by 40% responsive to a decrease in the amplitude of 25%
followed by their return to their initial values.
13. A device according to claim 12 wherein said mutual interaction
results in specific amplitude and pulse width values which is
plotted would approximate the A-gamma-motor strength duration curve
associated with the nerve being stimulated.
14. A device according to claim 13 wherein said pulse width
increases in response to a decrease in amplitude until said pulse
width reaches the A-delta-pain line.
15. A device according to claim 1 wherein said prescribed manner
includes mutual interaction between said amplitude control means
and said pulse width control means and has a modulation cycle of
six seconds, said modulation cycle being the time of the rate
modulation as well as the time involved in the mutual interaction
between the pulse width control means and the amplitude control
means.
Description
FIELD OF THE INVENTION
This invention relates to transcutaneous nerve stimulation and more
particularly to a transcutaneous nerve stimulating device which
represents an advancement in the suppression of organic pain.
BACKGROUND OF INVENTION
This invention is directed to the providing of a transcutaneous
nerve stimulator which is designed to be utilized in T.E.N.S.
(Transcutaneous Electrical Nerve Stimulation) therapy. T.E.N.S.
therapy is based on a non-invasive, non-narcotic concept of pain
management which is non-addictive, is not subject to abuse, and
does not interact with drugs. T.E.N.S. therapy has already proven
to be an effective modality in treating the organic pain problems
associated with the following conditions: chronic lumbar and
cervical strains or sprains, degenerating disc disease,
degenerative arthritic disease, neuropathies, neuralgias,
post-lumbar laminectomy syndrome, post-thoracotomy syndrome,
bursitis, postphlebitis syndrome, phantom limb syndrome, and
tension and migraine headaches.
Early attempts to suppress organic pain and other neurophysical
effects utilizing electrical stimulation occurred as early as about
2,000 years ago when it was discovered that gout apparently cuold
be successfully treated by placing the diseased extremities in a
tub of water filled with electric eels. Later, headaches were
treated using a similar approach. A detailed, scientific
investigation was finally conducted by Professor Galvani of the
University of Bologna, which investigation is credited with
ultimately leading to the development in the 1800's of electrical
equipment for suppression of organic pain.
The earliest therapeutic devices utilizing electrical simulation
for the most part featured a constant amplitude and rate. Examples
of the early art are Benz, U.S. Pat. No. 646,793; Raymond et. al.,
U.S. Pat. No. 872,148; Tibbals, U.S. Pat. No. 1,059,090; and Call,
U.S. Pat. No. 1,908,688. A major problem with electrical
stimulation therapy was, and still is, accommodation, whereby the
nerve being stimulated in effect accommodates itself over time to
the electrical charge, such that the effectiveness of the treatment
is diminished.
It took scientists a long time to discover, and attempt to address
the problem. Nemec, U.S. Pat. No. 2,622,601; DiPerma, U.S. Pat. No.
2,624,342; and Gratzl, U.S. Pat. No. 2,771,554 all disclose
electrotherapeutic devices with at least one including means to
vary the rate, amplitude or pulse width of the generated electrical
pulse. However, merely being able to change either the rate,
amplitude or pulse width still resulted in the problem of
accommodation occurring, unless an individual manually adjusted the
controls prior to the occurrence of accommodation. The process was
both labor intensive and inefficient, with respect to the quality
of the therapy, since maximum pain relief was not being
provided.
In 1967, a Dr. Sweet at Massachusetts General Hospital developed
the first T.E.N.S. unit. The effectiveness of T.E.N.S. therapy is
based on its incorporating two major pain control theories. Under
the so-called Gate Control Theory, pain can be inhibited and
suppressed by "closing the gate" on pain signals as such signals
arrive at Central Nervous System centers. This theory postulates
that by providing electrical stimulation of a sufficiently high
amplitude, the electrical signals race up large myelinated fibers
faster than the pain signals travel up smaller myelinated or
unmyelinated fibers. The neutral impulses transmitting pain
information to the brain thus become interrupted, and since the
brain fails to receive the pain signals, no pain is perceived. The
other theory incorporated in T.E.N.S. units is the Endorphin
Theory, also known as the Endogenous Opiate Theory. This theory
postulates that the sustained input of T.E.N.S. signals triggers
the release of naturally occurring pain making endorphins and
enkephalins (morphine-like substances). These natural substances
seemingly block pain signals by a mechanism similar to conventional
drug therapy, and inhibit pain information from reaching the
brain.
However, T.E.N.S. units, like all electrotherapeutic devices, have
suffered problems with accommodation. For example, Geerling, U.S.
Pat. No. 4,019,519 issued in 1977, disclosed a unit having only its
amplitude adjustable. Miller, U.S. Pat. No. 4,084,595 issued in
1978, disclosed a unit having its rate, amplitude, and pulse width
all independently, manually adjustable. However, even this
advancement resulted in a less than efficient treatment of the
problem of accommodation, since either the therapist or the patient
had to, in theory, repeatedly adjust the controls in an attempt to
avoid accommodation.
Although variation enables one to deal with the problem of
accommodation, pain relief is sacrificed. This is in part due to
the interaction between amplitude and pulse width. There is a
clinical correlation between amplitude and pulse width with regard
to the efficacy of the stimulus. As one shortens the duration of a
pulse, its amplitude must be increased to maintain the efficacy of
the stimulus. This relationship when plotted graphically is known
as a strength-duration curve. Thus not only must the ideal T.E.N.S.
units have adjustable amplitude and pulse width, but it must also
be able to modulate those values in such a way as to approximate
the A-gamma-motor strength-duration curve.
In addition to amplitude and pulse width approximating the
strenght-duration curve, the rate of the pulses must vary so as to
eliminate any potential for accommodation. This explains the
short-comings in Reiner, U.S. Pat. No. 2,808,826 which disclosed a
unit which permitted instantaneous changes in pulse width and
amplitude to two pre-set points along the strength-duration curve,
and Maurer, U.S. Pat. No. 4,340,063 which disclosed a unit having
its amplitude modulate in response to modulations in pulse width so
as to approximate a portion of the strength-duration curve. The
rate in Maurer was adjustable, but only to the extent taught by
Miller, such that the problem with accommodation still existed.
SUMMARY OF THE INVENTION
In accordance with this invention, a transcutaneous nerve
stimulator is provided for advantageous use in T.E.N.S. therapy. In
accordance with this invention, the amplitude, pulse width and rate
all modulate with respect to one another so as to obviate any
potential for the phenomenon of accommodation.
Included in the stimulator are a plurality of circuits, designed
such that the unit may operate in any one of five modes: burst,
conventional single amplitude/single pulse width, rate modulated,
amplitude modulated, and strength-duration/rate modulated. In this
final mode, the coordinated amplitude and pulse width approximate
the selected nerve's strength-duration curve. A Schmidt Trigger
serves to generate pulses, with at least one of the controls for
amplitude, pulse width and rate being independently adjustable for
the first four modes and with all three control means having their
respective values modulate when in the fifth mode. In this fifth
mode the amplitude control means and pulse width control means are
electrically coupled, with the rate control means interacting with
the product of the coupling, so as to provide maximum sensory
stimuli and maximum pain relief while eliminating the phenomenon of
accommodation.
The primary objective of this invention is to provide a nerve
stimulating device for use in T.E.N.S. therapy that eliminates the
phenomenon of accommodation. Important aspects of this objective
are the approximation of a nerve's strength-duration curve and the
additional effect caused by having the rate modulated so as to
interact with the curve generated by the interaction of amplitude
and pulse width.
Another object is the providing of a T.E.N.S. unit which can
provide a plurality of operating modes, including one for
strength-duration/rate. This important objective is furthered by
the providing of several circuits and selectively adjustable mode
control means which permits any one of five operating modes to be
chosen.
Still another objective is to provide a T.E.N.S. unit having all
the capabilities of this invention that is of extremely economical
construction and is particularly easy to operate. This objective is
furthered by supplying a T.E.N.S. unit having all the
chartacteristics of this invention as a portable, handheld
unit.
These and other objects and advantages of this invention will be
readily apparent from the following detailed description of an
illustrative embodiment thereof. Reference will be had to the
accompanying drawings which illustrate the embodiment of the
invention.
DESCRIPTION OF THE DRAWING FIGURES
FIG. 1 is a perspective view of a transcutaneous nerve stimulator
in its operative condition, showing the various controls.
FIG. 2 is a diagram of strength-duration curves for various classes
of nerve fibers.
FIG. 3 is a diagram similar to FIG. 2 but showing the phenomenon of
accommodation.
FIG. 4 is a diagram showing the effect of conventional modulation
of either amplitude or pulse width.
FIG. 5 is a diagram showing the effect of strength-duration
modulation.
FIG. 6 is a schematic diagram of the circuitry used in the
preferred embodiment.
DESCRIPTION OF THE ILLUSTRATIVE EMBODIMENT
Having reference to the drawings, attention is directed first to
FIG. 1 which illustrates a transcutaneous nerve stimulator
embodying this invention and designated generally by the numeral
10. This T.E.N.S. unit 10 has a base 11 and cover 12 which are
slidably interconnected, such that when the unit is in use the
cover 12 is slidably displaced to reveal front display panel 13.
The front display panel 13 features several adjustable control
means. Mode selector 14 permits the unit 10 to operate in five
distinct modes. Indicator lights 15,16,17,18, and 19 correspond to
burst, normal or conventional single amplitude/single pulse width,
rate modulated, amplitude modulated and strength-duration/rate
modulated modes, with a specific light being activated in response
to the mode selected. The indicator lights permit the user to know
what mode the unit 10 is in for reasons of safety. Also on the
front display panel 13 are rate and pulse width control means 20
and 21 respectively.
The unit 10 also features a top display panel 22 featuring two
amplitude control means 23 and 24, each of which are associated
with an electrode which is attached to the skin of the patient.
Electrode outlets (not shown) are located on the base 11 adjacent
to the rear of top display panel 22. Also located there is a low
battery light (not shown) which serves to apprise the user of the
charge conditions of the energy source used to power the
transcutaneous nerve stimulator of this invention.
Referring to FIG. 2, sensory, motor and pain thresholds are
illustrated by strength duration curves 30, 31, 32 and 33. Each
curve shows the effect of a specific pulse width and amplitude on
the firing of a particular class of nerves. When the
A-alpha-beta-sensory curve is intersected, that class of nerves
experiences a tingling sensation due to the current flow through
those nerves. When the A-gamma-motor curve is intersected, that
class of nerves experiences muscle fasciculation. When the
a-delta-pain or C-fibers-pain curves are intersected, those classes
of nerves experience discomfort which the individual perceives as
pain. The horizontal coordinate is a measurement of stimulus pulse
width, while the vertical coordinate is a measurement of stimulus
amplitude. Curve 30 corresponds to the A-alpha-beta-sensory curve.
Curve 31 corresponds to the A-gamma-motor curve. Curve 32
corresponds to the A-delta-pain curve. Curve 33 corresponds to the
C-fibers-pain curve. Ideally the level of stimulation should be
just below the level of muscle fasciculation (the A-gamma-motor
curve) as well as below the level of any pain.
As shown in FIG. 3, a T.E.N.S. unit may be adjusted to generate
pulses having a single amplitude and single pulse width 35 at a
level of ideal stimulation. However, with extended use, problems
occur due to accommodation. The phenomenon of accommodation results
in the nerve being stimulated requiring a greater degree of
stimulation as time passes, due to the nerve become depolarized and
hence less sensitive to stimuli.
One way to deal with the problem of accommodation has traditionally
been to modulate either the amplitude or the pulse width in a
decreasing fashion as shown in FIG. 4. By decreasing the amplitude
from that of point 35 to point 36, or by decreasing the pulse width
from that of point 35 to point 37, the problem of accommodation is
lessened, however the efficiency of the pain suppression is also
compromised.
According to this invention, a T.E.N.S. unit is provided which can
operate in a burst mode, the three modes shown in FIGS. 3 and 4
plus in a fifth mode wherein the phenomenon of accommodation is
obviated. In this new mode the amplitude and pulse width modulate
from point 25 to point 38 in a predetermined manner such that the
values for the amplitude and pulse width when in this mode are
shown in curve 39, which approximates the strength-duration curve
31. In this new mode, while the amplitude and pulse width are
responding to each other as shown in FIG. 5, the rate of the
generated pulses is also modulating. Utilization of the unit 10 in
the fifth mode eliminates problems with accommodation since the
nerves are allowed to relax and therefore re-polarize.
Now that the general physical and operational features of the
apparatus 10 have been described, consideration will now be given
to the electrical circuitry used in implementing the preferred
embodiment.
Referring to FIG. 6 the pulses for this invention are generated by
five of the gates of a Schmidt Trigger, while the sixth gate
toggles a low battery indicator. Choice of which of the five gates
are operating is determined by switch 50. When the switch is in
position A, the unit 10 is in burst mode. This mode exhibits the
same net effect quantitatively and qualitatively as the normal mode
setting. However the clinical effect is that fasciculation should
occur at lower amplitude settings, thus providing for a comfortable
sensation during treatments. Position A utilizes gates 51 and 55.
Gate 51 is trimmed to 2 Hz by a 500K resistance trimmer 52. Input
into oscillator 51 is driven by a 6.8 mf capacitor 53 such that the
resistance capacitance timing network is accomplished by the first
trimmer and capacitor.
Coupling from gate 51 to 85 Hz oscillator 55 is achieved by diode
56 located between pins 57 and 58. A capacitor 59 and 10K trimmer
60 allow gate 55 to produce a 85 Hz signal. Both trimmers 52 and 60
are fixed after adjusting them to specified parameters. Diode 61
and 68K fixed resistor between points 63 and 57 insert 7 pulses
into gate 55 twice each second.
Transistor switch 65 coupled gate 55 output signal through pin 66
into the gate of field effect transistor 70 when the switch 50 is
in position A. Switch position A also puts to ground both
capacitors 53 and 59 associated with gates 51 and 55, to activate
those two gates of the Schmidt Trigger integrated circuit. Switch
position A also grounds the base of pnp transistor 65 through a 68K
fixed resistor 71. A 470K fixed resistor 72 located at the base of
transistor 65 permits a regulated 5V signal to pass through it when
the switch is in position A. When another switch position is used,
capacitors 53 and 59 are lifted from ground, thereby closing gates
51 and 55. The presence of diode 73 helps to ensure that when gates
51 and 55 are shut off, the burst signals are prevented from
reaching field effect transistor 70. When the switch is not in
position A, diode 73 allows a small positive voltage to reach gate
51, holding both it and gate 55 from floating. Diode 73 has no
effect on the gates when the switch is in position A, such that the
pulse signals reach the gate of transistor 70 via transistor 65.
Switch position A also grounds the base of transistor 75 through
diode 76, as well as LED 77 which light indicates on the front
display panel 13 that the unit is operating in burst mode.
Switch position B permits operation of the unit 10 in the
conventional or normal single amplitude/single pulse width mode. In
this mode on this unit the rate, amplitude and pulse width all are
manually adjustable, however there is no modulation. When the
switch 50 is in position B the input of oscillator 80 through 68K
fixed resistor 81 is grounded. This prevents oscillator 80 from
operating. Preferably this Schmidt Trigger gate uses a 6 second
oscillator. In position B the base of transistor 75 is pulled high
through 470K fixed resistor 83 on the 5V supply 85, thereby
allowing the signal from oscillator 87 to reach the gate of
transistor 70.
The pulse width adjustment trimmers to 5V supply 85 are preferably
for minimum and maximum parameters of 30 and 225 micro seconds
respectively through the network of a 0.001 mf coupling capacitor
88 at the input of gate 90 of the Schmidt Trigger. The 0.001 mf
capacitor is driven by the drain of transistor 70, with the pulse
rate being coupled to the input of gate 90 through capacitor 88.
Pulse width is adjusted by 470K variable resistor 92 after trimming
the minimum and maximum parameters. The maximum is adjusted through
the use of 500K trimmer 93 or pin 94 through the 330K fixed
resistor 95 to pin 96 and thence to gate 90. The minimum is
adjusted through the 22K fixed resistor 97 and through the 500K
variable and 120 fixed resistors 98 and 99 respectively to the 5V
supply 85. A 10K fixed pull-up resistor 100 is located on the 5V
supply to the drain of transistor 70.
The rate is trimmed by 10K trimmer 110 located between pins 111 and
112 such that the maximum is 110 pulses per second. The minimum
rate is adjusted by a 500K trimmer 113 located between 470K fixed
resistor 114 and pin 115, such that the minimum is 1 pulse per
second. After setting the minimum and maximum parameters,
adjustment to the rate is obtained by a 470K potentiometer 120 with
the wiper of said potentiometer 120 through a 56K fixed resistor
121 tied to the 5V supply 85. This variable resistor divider
network allows the base of transistor 122 to offset, thereby making
it easier to read the values on rate adjustment knob 20. Turning
knob 20 results in potentiometer 120 causing a non-linear
adjustment to the rate. A 3.3 mf capacitor is located between the
emitter of transistor 122 and ground. When the switch 50 is in
position B, LED 124 is in an "on" condition, indicating the unit is
in the normal mode.
Switch position D permits the 6 second oscillator 80 to again
function by lifting from ground the 68K fixed resistor 81, allowing
the 6.8 mf capacitor 125 to change the resistance capacitance
network at oscillator 80 with a 2M fixed resistor 126 allowing
transition between high and low states. Gate 80 of the Schmidt
Trigger connects to 180K resistor 127 which is connected to diode
128. This circuit is connected to one having 10 mf capacitor 129 at
pin 130. Located between pin 130 and 2 m resistor 126 is 180K
resistor 131. Fixed resistors 127 and 131, diode 128 and capacitor
129 slow the transition of gate 80 to allow the gate of field
effect transistor 132 to be driven through a 2M resistor 134 tied
to ground to deplete the charge of the capacitor 129 as the gate 80
is driven high to low.
When the switch 50 is in position D, transistor 132 adds the 3.3 mf
capacitor 135 to gate 87 of the 1 to 110 Hz oscillator, thereby
decreasing the rate of the output pulses by approximately 50%,
regardless of the setting of potentiometer 120. As the gate 80
transcends from low to high, gate 132 is driven high to low
allowing the drain through switch position D to reach ground. The
source of transistor 132 with capacitor 135 is added and depleted
during the transition of gate 80 from high to low. At gate 87,
capacitor 135 is decreasing the rate by approximately 50% followed
by its return to the initial rate. Switch position D also grounds
LED 136 to an "on" position, thereby indicating that the unit is
operating in the rate modulation mode.
Switch position C connects the emitter of transistor 137 to ground.
The base of transistor 137 through 47K resistor 138 and three
voltage dropping diodes 139, 140 and 141 is driven from high to low
from the output of oscillator 80. The 470K fixed resistor 142 on
the cathode side of the three diodes 139,140 and 141 is driven from
high to low from the output of oscillator 80. The 470K fixed
resistor 142 on the cathode side of the three diodes 139, 140 and
141 is a feedback resistor, feeding the base of transistor 137. The
collector of transistor 137 also pulls the output signal of gate 90
through 4.7 fixed resistor 143, 3.3 K fixed resistor 144, and the
two 56K fixed resistors 145 and 146. The network of the four fixed
resistors 143, 144, 145 and 146 decreases the output signal through
the two 56K resistors 145 and 145 into the input of the operational
amplifiers 147 and 148 respectively by 25%, which is the preferred
amount of decrease for this invention.
Amplitude is further controlled by standard feedback loop balanced
amplifiers 147 and 148. Output is variable to 60 milliamps through
10K variable resistors 149 and 150 and is clamped at 150V and
filtered by 0.0047 mf capacitors 151 and 152. Two 39 pf capacitors
153 and 154 are utilized for noise reduction. Both channels use npn
transistors 155 and 156 respectively, with the collector of each
transistor connected to transformers 157 and 158 respectively.
Between the transformers and the electrode jacks 159 and 160 are
10K resistors 161 and 162 and LEDS 163 and 164. 390 ohm resistors
165 and 166 are located between amplifiers 147, 148 and transistors
155, 156. Adjustability of the amplitude for each electrode channel
is controlled by 20K potentiometers 167 and 168, with pins 169 and
170 located between the amplifiers 147, 148 and the potentiometers
167, 168. Also located between variable resistors 149, 150 and
potentiometers 167, 168 are pins 171 and 172 which go to ground.
Located between the amplifers and the capacitors 153, 154 and 120 K
fixed resistors 173 and 174. Between capacitors 153, 154 and the
emitters of transistors 155, 156 are 1K fixed resistors 175 and
176. Before going to ground, the current from transistors 155 and
156 passes through 0.27 ohm resistors 187 and 188 respectively.
Transformer 158 is provided with a 9V power supply 190. Switch
position C also grounds LED 194 to an "on" condition, indicating
that the unit is operating in an amplitude modulation
condition.
Switch position E results in a mode not heretofore available in
T.E.N.S. units. Features of switch positions C and D are
incorporated into the circuit associated with position E. A pair of
Germanium diodes 200 and 201 connect circuit D to E and C to E
respectively, with a 10K fixed pull-up resistor 203 connected to 5V
power supply 85 allowing for a current flow to bias the Germanium
diodes. Pin 204 is located between switch C and diode 201. The
emitter of transistor 205 through 2.2K resistor 206 to position E
is to ground. This allows 27K resistor 207 to decrease the 0.001 mf
capacitor 88 on the drain of transistor 70 by 40%. This decreases
the pulse width by 40% while not altering the rate. The 330K fixed
resistor 208 on the base of transistor 205 returns the base to
normal when not being high by the output of gate 80 through the
470K resistor 209 to the base. Thus when the unit 10 is in this
mode, rate modulation is occurring at the same time as is
amplitude/pulse width modulation.
In actual operation the initial component of the 6 second
oscillation involves a dramatic 50% decrease in the rate followed
by a return of the rate to its initial value during which time the
amplitude and pulse width modulate such that as the amplitude
decreases by 25% the pulse width increases by 40%. Once point 38 is
reached, as the amplitude increases to its initial value the width
decreases to its initial setting. Once the amplitude and pulse
width have returned to their original settings the next 6 second
oscillation occurs. LED 210 when in an "on" position indicates the
unit 10 is in the strength duration/rate modulation mode.
LED's 77, 124, 136, 194 and 210 are tied to a 2.2K fixed current
limiting resistor 213. Power supply 85 is regulated to 5V by
regulator 215. A 330 mf capacitor 216 is directly across the
battery potential. Also located in the LED circuit between power
supply 85 and regulator 215 is capacitor 217. Diode 218 is adjacent
battery 219 and serves to prevent damage to the unit in cases of
accidental battery reversal. The final gate 225 activates low
battery light LED 226 in cases when the power falls below 5V due to
a weakened battery. Preferably this diode will emit a color of
light different from the other LEDs.
A 0.033 mf capacitor 227 from the 9V battery 219 initializes gate
225 to pull that gate high, thereby preventing LED 226 from being
lighted. A 0.001 mf capacitor 228 from the regulated 5V power
supply 85 helps to keep electronic noise from gate 225. Current
flow through 10K resistor 229 causes LED 230 to emit preferably a
red color thereby providing a signal that the battery has some
charge left. However, the occasion may arise Cwhere the power in
the battery falls below 6V. In that situation it is safer for the
use of the unit to be interrupted and the battery to be
replaced.
The interruption occurs when the divide network including 330K and
470K resistors 235 and 236 respectively falls to 6V. At that time
the input of gate 225 which is normally high, goes to ground
through 20K resistor 237 and transistor 238. Also at this time
current through 120K resistor 239 closes gate 225. Once current
flows through and closes gate 225, diode 226 becomes lit, in
addition to current flowing through 1K resistor 240 to diodes 241
and 242 which are connected to operating amplifiers 147 and 148
respectively. The passage of current through these diodes shuts
down the amplifiers, thereby preventing the unit from functioning.
This situation continues until the battery is replaced, at which
time the input to gate 225 will once again be high, such that no
current will be flowing to diodes 241 and 242.
It will be readily apparent, from the foregoing detailed
description of the preferred embodiment of this invention, that a
particularly novel and extremely effective T.E.N.S. device is
provided. This device is relatively simple to fabricate and results
in a device which provides a degree of relief heretofore unknown in
the treatment of pain.
* * * * *